Tag: M.W=300-350

Yart, Lucile published the artcileDual effect of nifedipine on pregnant human myometrium contractility: Implication of TRPC1, HPLC of Formula: 21829-25-4, the publication is Journal of Cellular Physiology (2022), 237(3), 1980-1991, database is CAplus and MEDLINE.

Nifedipine, an L-type voltage-gated Ca²⁺ channel (L-VGCC) blocker, is one of the most used tocolytics to treat preterm labor. In clin. practice, nifedipine efficiently decreases uterine contractions, but its efficacy is limited over time, and repeated or maintained nifedipine-based tocolysis appears to be ineffective in preventing preterm birth. We aimed to understand why nifedipine has short-lasting efficiency for the inhibition of uterine contractions. We used ex vivo term pregnant human myometrial strips treated with cumulative doses of nifedipine. We observed that nifedipine inhibited spontaneous myometrial contractions in tissues with high and regular spontaneous contractions. By contrast, nifedipine appeared to increase contractions in tissues with low and/or irregular spontaneous contractions. To investigate the mol. mechanisms activated by nifedipine in myometrial cells, we used the pregnant human myometrial cell line PHM1-41 that does not express L-VGCC. The in vitro measurement of intracellular Ca²⁺ showed that high doses of nifedipine induced an important intracellular Ca²⁺ entry in myometrial cells. The inhibition or downregulation of the genes encoding for store-operated Ca²⁺ entry channels from the Orai and transient receptor potential-canonical (TRPC) families in PHM1-41 cells highlighted the implication of TRPC1 in nifedipine-induced Ca²⁺ entry. In addition, the use of 2-APB in combination with nifedipine on human myometrial strips tends to confirm that the pro-contractile effect induced by nifedipine on myometrial tissues may involve the activation of TRPC channels.

Journal of Cellular Physiology published new progress about 21829-25-4. 21829-25-4 belongs to pyridine-derivatives, auxiliary class Membrane Transporter/Ion Channel,Calcium Channel, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C28H29NO4, HPLC of Formula: 21829-25-4.

Referemce:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Shahzadi, Hafiza Tayyaba published the artcileIridium-Catalyzed C-H Borylation of CF₃-Substituted Pyridines, Application In Synthesis of 741709-67-1, the publication is ACS Omega (2022), 7(13), 11460-11472, database is CAplus and MEDLINE.

Iridium-catalyzed C-H borylation of CF₃-substituted pyridines is described in this paper. The boronic ester group can be installed on the α, β, or γ position of pyridine by an appropriate substitution pattern. Sterically governed regioselectivity provides convenient access to a variety of CF₃-substituted pyridylboronic esters. These catalytic C-H borylation reactions were carried out neatly without the use of any solvent. Several functional groups, such as halo, ester, alkoxy, amino, etc., are compatible with this methodol. These pyridylboronic esters are amenable to column chromatog. and the products were isolated in good to excellent yields. α-Borylated pyridines, although isolated in good yields, do not have a long shelf life. The boronic ester derivatives of these CF₃-substituted pyridines can serve as useful precursors in the synthesis regime.

ACS Omega published new progress about 741709-67-1. 741709-67-1 belongs to pyridine-derivatives, auxiliary class Trifluoromethyl,Pyridine,Fluoride,Chloride,Boronic acid and ester,Boronate Esters,Boronic Acids,Boronic acid and ester, name is 2-Chloro-5-(4,4,5,5-tetramethyl-1,3,2-dioxaborolan-2-yl)-3-(trifluoromethyl)pyridine, and the molecular formula is C12H16BBrO2, Application In Synthesis of 741709-67-1.

Referemce:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Zhou, Su published the artcileOptimization for the coating prescription of porosity osmotic pump-controlled release tablets of betahistine mesilate, Recommanded Product: N-Methyl-2-(pyridin-2-yl)ethan-1-amine dimethanesulfonate, the publication is Zhongguo Yaofang (2011), 22(21), 1970-1972, database is CAplus.

The aim of this paper is to prepare porosity osmotic pump-controlled release tablets of betahistine mesilate, and optimize the coating prescription. Main influencing factors for drug release of porosity osmotic pump-controlled release tablets were investigated with single factor experiment The coating prescription was optimized by orthogonal test with the amount of PEG and DBP as factors and drug release indicator L as index. Similar factor was less than 50 which indicated that the amount of PEG, DBP and coating level affected the in vitro drug release significantly. The optimized coating prescription was as follows: PEG 30%, DBP 20% and the weight increment of coating material 4%. The drug release indicators of 3 batches of samples in validation test were 13.99, 11.15 and 8.37. Accumulative drug release rate was more than 90% within 12 h, and the drug release model showed zero-level drug release characteristics. Porosity osmotic pump-controlled release tablets of betahistine mesilate with optimized prescription can achieve constant complete release in 12 h.

Zhongguo Yaofang published new progress about 54856-23-4. 54856-23-4 belongs to pyridine-derivatives, auxiliary class Pyridine,Salt,Amine,Inhibitor,Inhibitor, name is N-Methyl-2-(pyridin-2-yl)ethan-1-amine dimethanesulfonate, and the molecular formula is C9H8O4, Recommanded Product: N-Methyl-2-(pyridin-2-yl)ethan-1-amine dimethanesulfonate.

Referemce:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Martins, Samantha Eslava published the artcileReview: ecotoxicity of organic and organo-metallic antifouling co-biocides and implications for environmental hazard and risk assessments in aquatic ecosystems, Related Products of pyridine-derivatives, the publication is Biofouling (2018), 34(1), 34-52, database is CAplus and MEDLINE.

A review. Hazard assessments of Irgarol 1051, diuron, 2-(thiocyanomethylthio)benzothiazole (TCMTB), dichloro-octylisothiazolin (DCOIT), chlorothalonil, dichlofluanid, thiram, zinc pyrithione, copper pyrithione, triphenylborane pyridine (TPBP), capsaicin, nonivamide, tralopyril and medetomidine were performed to establish robust environmental quality standards (EQS), based on predicted no effect concentrations (PNECs). Microalgae, zooplankton, fish and amphibians were the most sensitive ecol. groups to all the antifoulants evaluated, especially in the early life stages. No differences were identified between freshwater and seawater species. The use of toxicity tests with non-standard species is encouraged because they increase the datasets, allowing EQS to be derived from probabilistic-based PNECs while reducing uncertainties. The global ban of tributyltin (TBT) has been heralded as a major environmental success; however, substitute antifoulants may also pose risks to aquatic ecosystems. Environmental risk assessments (ERAs) have driven decision-makings for regulating antifouling products, but in many countries there is still a lack of regulation of antifouling biocides which should be addressed.

Biofouling published new progress about 971-66-4. 971-66-4 belongs to pyridine-derivatives, auxiliary class Pyridine,Benzene, name is Triphenyl(pyridin-1-ium-1-yl)borate, and the molecular formula is C23H20BN, Related Products of pyridine-derivatives.

Referemce:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Hughes, Rebecca E. published the artcileMultiparametric High-Content Cell Painting Identifies Copper Ionophores as Selective Modulators of Esophageal Cancer Phenotypes, Synthetic Route of 54856-23-4, the publication is ACS Chemical Biology (2022), 17(7), 1876-1889, database is CAplus and MEDLINE.

Esophageal adenocarcinoma is of increasing global concern due to increasing incidence, a lack of effective treatments, and poor prognosis. Therapeutic target discovery and clin. trials have been hindered by the heterogeneity of the disease, the lack of “druggable” driver mutations, and the dominance of large-scale genomic rearrangements. We have previously undertaken a comprehensive small-mol. phenotypic screen using the high-content Cell Painting assay to quantify the morphol. response to a total of 19,555 small mols. across a panel of genetically distinct human esophageal cell lines to identify new therapeutic targets and small mols. for the treatment of esophageal adenocarcinoma. In this current study, we report for the first time the dose-response validation studies for the 72 screening hits from the target-annotated LOPAC and Prestwick FDA-approved compound libraries and the full list of 51 validated esophageal adenocarcinoma-selective small mols. (71% validation rate). We then focus on the most potent and selective hit mols., elesclomol, disulfiram, and ammonium pyrrolidinedithiocarbamate. Using a multipronged, multitechnol. approach, we uncover a unified mechanism of action and a vulnerability in esophageal adenocarcinoma toward copper-dependent cell death that could be targeted in the future.

ACS Chemical Biology published new progress about 54856-23-4. 54856-23-4 belongs to pyridine-derivatives, auxiliary class Pyridine,Salt,Amine,Inhibitor,Inhibitor, name is N-Methyl-2-(pyridin-2-yl)ethan-1-amine dimethanesulfonate, and the molecular formula is C10H20N2O6S2, Synthetic Route of 54856-23-4.

Referemce:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Adel Madbouly, Neveen published the artcileIn vitro and in vivo impacts of nifedipine and diltiazem on praziquantel chemotherapy in murine Schistosoma mansoni, Application of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the publication is Experimental Parasitology (2022), 108256, database is CAplus and MEDLINE.

This study was planned to evaluate the in vitro and in vivo antischistosomal effects of the widely used antihypertensive drugs, nifedipine (NIF) and diltiazem (DTZ), and their combinations with praziquantel (PZQ) on early and late Schistosoma (S.) mansoni infections 21- and 45- days old stages. In the In vitro study, Calcium channel blockers (CCBs), NIF and DTZ were added to schistosomula and adult worm cultures in different concentrations 10, 20 and 30 mg/mL. The mortality percentage was calculated 1, 12 and 24 h after incubation. In vivo, NIF and DTZ either alone or combined with PZQ were used to treat male albino mice. The parasitol. and total Ig (Ig) G and IgM anti-soluble egg antigen (SEA) were assessed to demonstrate the disease severity. In the In vitro study, 10 mg/mL NIF induced 100% mortality percentage of both schistosomula and adult worms after 24 h incubation, while DTZ induced similar mortality percentage at 30 mg/mL concentration In vivo results showed that early or late combination of 30 mg/kg of NIF, but not DTZ, significantly (P <0.05) enhanced the reductive efficacy of PZQ based on the parasitol. data. The maximal reduction (P <0.05) of anti-SEA IgM and IgG levels was developed during NIF-PZQ administration 21- (1.12 ± 0.06 and 1.09 ± 0.04, resp.) or 45- (1.00 ± 0.03 and 0.8 ± 0.06, resp.) days post infection (PI), compared to either PZQ or NIF individual treatments. The decreased concentration of anti-SEA antibodies was correlated with the diminished granulomatous diameter and disease severity. Nifedipine improved PZQ chemotherapy targeting either early or late S. mansoni infection in mice compared to the PZQ mono-therapy. Administering NIF can be considered as a promising drug candidate for schistosomiasis chemotherapy.

Experimental Parasitology published new progress about 21829-25-4. 21829-25-4 belongs to pyridine-derivatives, auxiliary class Membrane Transporter/Ion Channel,Calcium Channel, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Application of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

Referemce:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Sarthou, Manon C. M. published the artcileCalcium-permeable cation channels are involved in uranium uptake in Arabidopsis thaliana, Category: pyridine-derivatives, the publication is Journal of Hazardous Materials (2022), 424(Part_B), 127436, database is CAplus and MEDLINE.

Uranium (U) is a non-essential and toxic element that is taken up by plants from the environment. The assimilation pathway of U is still unknown in plants. In this study, we provide several evidences that U is taken up by the roots of Arabidopsis thaliana through Ca²⁺-permeable cation channels. First, we showed that deprivation of Arabidopsis plants with calcium induces a 1.5-fold increase in the capacity of roots to accumulate U, suggesting that calcium deficiency promotes the radionuclide import pathway. Second, we showed that external calcium inhibits U accumulation in roots, suggesting a common route for the uptake of both cations. Third, we found that gadolinium, nifedipine and verapamil inhibit the absorption of U, suggesting that different types of Ca²⁺-permeable channels serve as a route for U uptake. Last, we showed that U bioaccumulation in Arabidopsis mutants deficient for the Ca²⁺-permeable channels MCA1 and ANN1 is decreased by 40%. This suggests that MCA1 and ANN1 contribute to the absorption of U in different zones and cell layers of the root. Together, our results describe for the first time the involvement of Ca²⁺-permeable cation channels in the cellular uptake of U.

Journal of Hazardous Materials published new progress about 21829-25-4. 21829-25-4 belongs to pyridine-derivatives, auxiliary class Membrane Transporter/Ion Channel,Calcium Channel, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Category: pyridine-derivatives.

Referemce:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Yadav, Rakhee published the artcileRole of calcium ion channels and cytoskeletal proteins in Thorium-232 induced toxicity in normal human liver cells (WRL 68) and its validation in swiss mice, Application In Synthesis of 21829-25-4, the publication is Chemosphere (2022), 288(Part_2), 132557, database is CAplus and MEDLINE.

Hepatic disorders reported in humans exposed to Thorium-232 (Th-232) rationalizes the present study investigating the toxicol. response of normal human liver cells (WRL 68) and its validation in Swiss mice. Cell count anal. of WRL 68 cells-treated with Th-nitrate (1-200μM) estimated IC₅₀ of ∼24μM (at 24 h) and 35μM (at 48 h). Anal. of cell viability (trypan blue assay) showed the IC₅₀ of ∼172μM. Phase contrast bright-field microscopy revealed Th-induced morphol. changes and cell-released microvesicle-like structures in extracellular space. Th-estimation by ICP-MS (Inductively-coupled plasma mass-spectrometry) showed uptake of Th by cells as a function of concentration and incubation time. Employing DTPA as a chelating agent in cell harvesting solution, cell-internalized/strongly-bound Th was estimated to be ∼42% of total incubated Th. Th-uptake studies in the presence of ion-channel specific inhibitors (e.g. nifedipine, thapsigargin) revealed the role of plasma membrane calcium channels and cytoplasmic calcium in modulating the Th-uptake. Transmission electron microscopy of Th-treated cells showed cell-derived extracellular vesicles, alterations in the shape and size of nucleus and mitochondria as well as cytoplasmic inclusions. The order of Th accumulation in various sub-cellular protein fractions was found to be as cytoskeleton (43%) > cytoplasmic (15%) > chromatin (7%) > nuclear (5%) & membrane (5%). Immunofluorescence anal. of WRL 68 cells showed that Th significantly altered the expression of cytoskeleton proteins (F-actin and keratin), which was further validated in liver tissues of Swiss mice administered with Th-232. Findings herein highlight the role of calcium channels and cytoskeleton in Th-induced toxicity. Keywords: Thorium toxicity; Liver cells; Calcium channels; Sub-cellular targets, Cytoskeleton; Swiss Mice.

Chemosphere published new progress about 21829-25-4. 21829-25-4 belongs to pyridine-derivatives, auxiliary class Membrane Transporter/Ion Channel,Calcium Channel, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C8H6KNO4S, Application In Synthesis of 21829-25-4.

Referemce:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Manz, Kevin M. published the artcileCocaine restricts nucleus accumbens feedforward drive through a monoamine-independent mechanism, Application of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the publication is Neuropsychopharmacology (2022), 47(3), 652-663, database is CAplus and MEDLINE.

Parvalbumin-expressing fast-spiking interneurons (PV-INs) within feedforward microcircuits in the nucleus accumbens (NAc) coordinate goal-directed motivational behavior. Feedforward inhibition of medium spiny projection neurons (MSNs) is initiated by glutamatergic input from corticolimbic brain structures. While corticolimbic synapses onto MSNs are targeted by the psychostimulant, cocaine, it remains unknown whether cocaine also exerts acute neuromodulatory actions at collateralizing synapses onto PV-INs. Using whole-cell patch-clamp electrophysiol., optogenetics, and pharmacol. tools in transgenic reporter mice, we found that cocaine decreases thalamocortical glutamatergic drive onto PV-INs by engaging a monoamine-independent mechanism. This mechanism relies on postsynaptic sigma-1 (σ1) activity, leading to the mobilization of intracellular Ca2+ stores that trigger retrograde endocannabinoid signaling at presynaptic type-1 cannabinoid receptors (CB1R). Cocaine-evoked CB1R activity occludes the expression of CB1R-dependent long-term depression (LTD) at this synaptic locus. These findings provide evidence that acute cocaine exposure targets feedforward microcircuits in the NAc and extend existing models of cocaine action on mesolimbic reward circuits.

Neuropsychopharmacology published new progress about 21829-25-4. 21829-25-4 belongs to pyridine-derivatives, auxiliary class Membrane Transporter/Ion Channel,Calcium Channel, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Application of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

Referemce:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Farfan, Norberto published the artcileCarbon-13 nuclear magnetic resonance spectroscopy as a method to determine relative acidity of boron Lewis acids in pyridine complexes, Application of Triphenyl(pyridin-1-ium-1-yl)borate, the publication is Journal of the Chemical Society, Perkin Transactions 2: Physical Organic Chemistry (1972-1999) (1987), 771-3, database is CAplus.

Complexes of pyridine and 2-ethylpyridine with a series of boron Lewis acids have been studied using ¹H, ¹¹B, and ¹³C NMR. The difference in chem. shifts (Δδ_c-4) between the boron complex and the free pyridine were correlated with calorimetric data. The ¹³C data show that Δδ_c-4 of pyridines provides a measure of the strength of the N → B bond, thus allowing a scale of acidity for boron compounds to be derived.

Journal of the Chemical Society, Perkin Transactions 2: Physical Organic Chemistry (1972-1999) published new progress about 971-66-4. 971-66-4 belongs to pyridine-derivatives, auxiliary class Pyridine,Benzene, name is Triphenyl(pyridin-1-ium-1-yl)borate, and the molecular formula is C23H20BN, Application of Triphenyl(pyridin-1-ium-1-yl)borate.

Referemce:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem